Nature cell biology · 2024
Solid tumour-induced systemic immunosuppression involves dichotomous myeloid-B cell interactions.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Hao Xiaoxin, Shen Yichao, Liu Jun, Alexander Angela, Wu Ling, Xu Zhan, Yu Liqun, Gao Yang, Liu Fengshuo, Chan Hilda L, Li Che-Hsing, Ding Yunfeng, Zhang Weijie, Edwards David G, Chen Nan, Nasrazadani Azadeh, Ueno Naoto T, Lim Bora, Zhang Xiang H-F
Аннотация
Solid tumours induce systemic immunosuppression that involves myeloid and T cells. B cell-related mechanisms remain relatively understudied. Here we discover two distinct patterns of tumour-induced B cell abnormality (TiBA; TiBA-1 and TiBA-2), both associated with abnormal myelopoiesis in the bone marrow. TiBA-1 probably results from the niche competition between pre-progenitor-B cells and myeloid progenitors, leading to a global reduction in downstream B cells. TiBA-2 is characterized by systemic accumulation of a unique early B cell population, driven by interaction with excessive neutrophils. Importantly, TiBA-2-associated early B cells foster the systemic accumulation of exhaustion-like T cells. Myeloid and B cells from the peripheral blood of patients with triple-negative breast cancer recapitulate the TiBA subtypes, and the distinct TiBA profile correlates with pathologic complete responses to standard-of-care immunotherapy. This study underscores the inter-patient diversity of tumour-induced systemic changes and emphasizes the need for treatments tailored to different B and myeloid cell abnormalities.